ABSTRACT
AIM:To investigate the effect of lutein on the viability of breast cancer cells and its possible mech -anism.METHODS:The human breast cancer T47D cells were divided into control group and lutein(6.25,12.5,25,50 mg/L)treatment groups.The effect of lutein on the viability of T47D cells was measured by MTT assay.The mRNA ex-pression of nuclear factor erythroid 2-related factor 2(Nrf2),glutathione peroxidase 1(GPx1)and superoxide dismutase 2 (SOD2)was detected by RT-qPCR.Fluorescent probes DCFH-DA was used to determine the production of reactive oxygen species(ROS).The protein expression of Nrf2 and p65 was determined by Western blot.RESULTS: The MTT results showed that lutein inhibited T47D breast cancer cell viability in a dose-and time-dependent manner.The RT-qPCR results showed that the mRNA levels of Nrf2, GPx1 and SOD2 were higher in lutein treatment groups than those in the control group(P<0.05),and with the increased concentrations and extension of intervention time of lutein, the relative mRNA levels were all increased.The ROS levels were significantly decreased in the lutein-treated groups(P<0.05).The results of Western blot demonstrated that the protein expression of Nrf 2 was significantly increased(P<0.05), and p65 protein was decreased(P<0.05)in a dose-dependent manner with lutein treatment for 48 h.CONCLUSION: Lutein signifi-cantly inhibits the viability of breast cancer cells,and the inhibition roles may be related to up-regulation of the expression of Nrf2,antioxidant enzymes GPx1 and SOD2 mRNA expression and down-regulation of oxidative stress,thus blocking the NF-κB signaling pathway.
ABSTRACT
<p><b>OBJECTIVE</b>To study the effects of lutein on apoptosis and its mechanism.</p><p><b>METHOD</b>The cells of human esophageal carcinoma EC9706 were grown in RPMI medium containing 10% bovine serum and were treated with lutein at 100 microg x mL(-1) concentration. Flow cytometry was employed to investigate the effects of lutein on cell apoptosis of EC9706 cells. Histochemistry was performed to determine apoptosis-related protein expresion.</p><p><b>RESULT</b>Flow cytometry analyses revealed that lutein increased EC9706 cell apoptosis ratio when treated with lutein 100 microg x mL(-1) at 96 h. Lutein decreased the expression of Bcl-2 protein and increased the expression of Bax protein in EC9706 cells.</p><p><b>CONCLUSION</b>Lutein could inhibit mitosis and stimulate apoptosis of EC9706 cells. The apoptotic effect may result from the down-regulation of expression of Bcl-2 and up-regulation expression of Bax.</p>
Subject(s)
Humans , Antineoplastic Agents, Phytogenic , Pharmacology , Apoptosis , Carcinoma, Squamous Cell , Metabolism , Pathology , Cell Line, Tumor , Esophageal Neoplasms , Metabolism , Pathology , Lutein , Pharmacology , Proto-Oncogene Proteins c-bcl-2 , Metabolism , bcl-2-Associated X Protein , MetabolismABSTRACT
<p><b>OBJECTIVE</b>To explore the mechanism of warming-needle therapy in treatment of knee osteoarthritis of deficiency-cold syndrome.</p><p><b>METHODS</b>Eight cases of knee osteoarthritis of deficiency-cold syndrome were selected and treated with warming-needle therapy at Guanyuan (CV 4), Qihai (CV 6) , Zosanli (ST 36), etc.. The gene expression profiles before and after treatment in 4 cases who showed better therapeutic effect were compared. Taking ratio < 0.5 or ratio > 2.0 as differentially expression gene and obtaining differentially expression pathway (P < 0.5, n>3) by http://www. DAVID 2006.</p><p><b>RESULTS</b>Two cases were clinically cured, 4 cases were markedly effective, 1 case was effective and 1 case was ineffective. With help of the microarray, 449 differentially expression genes, and 10 differentially expression pathways were obtained including 2 energy metabolism pathways (oxidative phosphorylation, ATP synthetase), 4 cell signal transduction pathways (insulin signal pathway, Toll-like receptor signal pathway, JAK-STAT signal pathway, and MAPK signal pathway) and cell apoptosis pathway.</p><p><b>CONCLUSION</b>Warming-needle therapy is an effective therapy for knee osteoarthritis with deficiency-cold syndrome , which is possibly involved in the control and regulation of many gene expression by various signal transduction pathways.</p>